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Документ Melatonergic Receptors (Mt1/Mt2) as a Potential Additional Target of Novel Drugs for Depression(Springer, 2022-06) Boiko, Dmytro I.; Shkodina, Anastasiia D.; Hasan, Mohammad Mehedi; Bardhan, Mainak; Kazmi, Syeda Kanza; Chopra, Hitesh; Bhutra, Prerna; Baig, Atif Amin; Skrypnikov, Andrii M.; Бойко, Дмитро Іванович; Шкодіна, Анастасія Дмитрівна; Скрипніков, Андрій МиколайовичA complex pathogenesis involving several physiological systems is theorized to underline the development of depressive disorders. Depression is accompanied by circadian regulation disruption and interaction with the functioning of both central and peripheral oscillators. Many aspects of melatonin function unite these systems. The use of drugs for circadian rhythm disorders could inspire a potential treatment strategy for depression. Melatonin plays an essential role in the regulation of circadian rhythms. It exerts effect by activating two types of melatonin receptors, type 1A (MT1) and 1B (MT2). These are G-protein-coupled receptors, predominantly located in the central nervous system. MT1/MT2 agonists could be a useful treatment approach according to all three prevalent theories of the pathogenesis of depression involving either monoamines, synaptic remodeling, or immune/inflammatory events. MT1/MT2 receptors can be a potential target for novel antidepressants with impact on concentrations of neurotrophins or neurotransmitters, and reducing levels of pro-inflammatory cytokines. There is an interesting cross-talk mediated via the physical association of melatonin and serotonin receptors into functional heteromers. The antidepressive and neurogenetic effects of MT1/MT2 agonists can also be caused by the inhibition of the acid sphingomyelinase, leading to reduced ceramide, or increasing monoamine oxidase A levels in the hippocampus. Compounds targeting MT1 and MT2 receptors could have potential for new anti-depressants that may improve the quality of therapeutic interventions in treating depression and relieving symptoms. In particular, a combined effect on MT1 and/or MT2 receptors and neurotransmitter systems may be useful, since the normalization of the circadian rhythm through the melatonergic system will probably contribute to improved treatment. In this review, we discuss melatonergic receptors as a potential additional target for novel drugs for depression.Документ Roles of clock genes in the pathogenesis of Parkinson's disease(Elsevier, 2022-02) Shkodina, Anastasiia Dmytrivna; Tan, Shing Cheng; Hasan, Mohammad Mehedi; Abdelgawad, Mai; Chopra, Hitesh; Bilal, Muhammad; Boiko, Dmytro Ivanovych; Tarianyk, Kateryna Anatoliivna; Alexiou, Athanasios; Шкодіна, Анастасія Дмитрівна; Бойко, Дмитро Іванович; Таряник, Катерина АнатоліївнаParkinson's disease (PD) is a common motor disorder that has become increasingly prevalent in the ageing population. Recent works have suggested that circadian rhythms disruption is a common event in PD patients. Clock genes regulate the circadian rhythm of biological processes in eukaryotic organisms, but their roles in PD remain unclear. Despite this, several lines of evidence point to the possibility that clock genes may have a significant impact on the development and progression of the disease. This review aims to consolidate recent understanding of the roles of clock genes in PD. We first summarized the findings of clock gene expression and epigenetic analyses in PD patients and animal models. We also discussed the potential contributory role of clock gene variants in the development of PD and/or its symptoms. We further reviewed the mechanisms by which clock genes affect mitochondrial dynamics as well as the rhythmic synthesis and secretion of endocrine hormones, the impairment of which may contribute to the development of PD. Finally, we discussed the limitations of the currently available studies, and suggested future potential studies to deepen our understanding of the roles of clock genes in PD pathogenesis.Документ Schizophrenia and disruption of circadian rhythms: An overview of genetic, metabolic and clinical signs(Elsevier, 2024) Boiko, D. I.; Chopra, Hitesh; Bilal, Muhammad; Kydon, P. V.; Herasymenko, L. O.; Rud, V. O.; Bodnar, L. A.; Vasylyeva, G. Yu.; Isakov, R. I.; Zhyvotovska, L. V.; Mehta, Aashna; Skrypnikov, A. M.; Бойко, Дмитро Іванович; Кидонь, Павло Володимирович; Герасименко, Лариса Олександрівна; Рудь, Вадим Олексійович; Боднар, Леся Анатоліївна; Васильєва, Ганна Юріївна; Ісаков, Рустам Ісроїлович; Животовська, Лілія Валентинівна; Скрипніков, Андрій МиколайовичA molecular clock in the suprachiasmatic nucleus of the anterior hypothalamus, which is entrained by the dark-light cycle and controls the sleep-wake cycle, regulates circadian rhythms. The risk of developing mental disorders, such as schizophrenia, has long been linked to sleep abnormalities. Additionally, a common aspect of mental disorders is sleep disturbance, which has a direct impact on the intensity of the symptoms and the quality of life of the patient. This relationship can be explained by gene alterations such as CLOCK in schizophrenia which are also important components of the physiological circadian rhythm. The function of dopamine and adenosine in circadian rhythm should also be noted, as these hypotheses are considered to be the most popular theories explaining schizophrenia pathogenesis. Therefore, determining the presence of a causal link between the two can be key to identifying new potential targets in schizophrenia therapy, which can open new avenues for clinical research as well as psychiatric care. We review circadian disruption in schizophrenia at the genetic, metabolic, and clinical levels. We summarize data about clock and clock-controlled genes' alterations, neurotransmitter systems' impairments, and association with chronotype in schizophrenia patients. Our findings demonstrate that in schizophrenia either homeostatic or circadian processes of sleep regulation are disturbed. Also, we found an insufficient number of studies aimed at studying the relationship between known biological phenomena of circadian disorders and clinical signs of schizophrenia.